Pharmacology in Pain Management Flashcards

1
Q

mild pain

A

(1-3)

-use step 1 drugs (NSAIDS & acetaminophen)

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2
Q

pain is a reflection of what?

A

emotion and attitude

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3
Q

R: region

A

where is it? does it stay there?

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4
Q

treatments

A

-2nd line:
Tryptans are serotonin/ 5-HT-1 receptors against that constrict intracranial vessels.
sumatriptans, zolmitriptan, rizatriptan, etc. (have various half-lives, times of onset)

some also come in combo, sumatriptan plus naproxin

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5
Q

tension headaches

A
  • dull quality, pain radiates to forehead, neck, shoulders
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6
Q

how do we assess pain?

A

PQRSTU

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7
Q

severe pain

A

(7-10)

-use opiates/ step 3 (morphine, hydromorphone/dilaudid, oxycodone/oxycontin, oxymorphone, Fentora)

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8
Q

Local anesthetics

A

sodium channel blockers that reduce pain impulses (novocaine)
(lidocaine)

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9
Q

transmission

A

through dorsal horn of cord; if signal is strong enough, may reach CNS, though there are inhibitory fibers in cord to reduce upstream signal

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10
Q

treatment of tension headache

A
  • acetaminophen & aspirin (1st line)
  • NSAIDS (2nd line)
    • can give antiemetics if accompanying nausea (promethazine/ prochlorperazine)
  • combination of meds: (3rd line)
  • Fioricet (butalbital/ acetaminophen/ caffeine)
  • Fiorinal (butalbital/ aspirin/ caffeine)
  • *** some anti-depressants also used, including amitriptyline, fluoxetine, others
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11
Q

chronic pain:

A
  • lasts over 3-6 months
  • pain persists after injury has healed
  • can be from a variety of tissues
  • perhaps the result of “neuroplasticity”
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12
Q

anti-convulsants

A

gabapentin & pregabalin activate GABA receptors & reduce neutotransmitters

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13
Q

acute pain

A

sudden onset & related to a specific case (trauma/damage)

  • can be accompanied by other physiological responses, (increased HR, sweating, rapid breathing)
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14
Q

Treating pain

A

mild pain
moderate pain
severe pain

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15
Q

what is pain?

A

Unpleasant sensory & emotional experience associated w/ actual or potential tissue damage

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16
Q

signal reducers

A

those that normally inhibit pain signals

-B-endorphin (mu receptors), NE, and GABA

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17
Q

what is pain pathophysiology?

A

transduction
transmission
perception
modulation

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18
Q

mediators or pain signals

A

PG’s, substance P (even stimulating second order neurons in cord)
bradykinins

19
Q

P: precipitating/ palliating

A

what makes it worse or better?

20
Q

treatments

A
-3rd line:
Ergot derivatives (ergotamine or dihydroergotamine)
lead to vasoconstriction
21
Q

Co-Analgesics for pain

A

Antidepressants
Anticonvulsants
Local Anesthetics
Muscle Relaxants

22
Q

Migraine triggers?

A
  • physiologic factors(anxiety, depression)
  • medications (hormones, nicotine, nitroglycerin)
  • diet (alcohol, caffeine, chocolate)
  • environment (light, altitude, odors, sounds, weather)
  • lifestyle (dieting, exercise, sleep patterns)
  • hormonal factors (pregnancy, menopause)
23
Q

transduction

A

A-delta nerves and C-nerves (fibers) are activated by PGs, substance P, histamine, etc

24
Q

modulation

A

inhibitory effects in the CNS to reduce the sense of pain in a descending pathway

25
moderate pain
(4-6) | -use NSAIDS plus opiates/ step 2 (hydrocodone/Vicodin, oxycodone/Percocet)
26
S: severity
Pain scales?
27
treatments
-1st line: (NSAIDS & aspirin) caffeine- containing meds (Excedrin (migraine))
28
perception
signals in both the cortex and limbic system = COGNITIVE & EMOTIONAL component
29
cluster headaches
disabling, burning, or boring feeling around one eye & extremely painful
30
migraine
head throbbing, nausea, photophobia, photophobia, and can be debilitating
31
Headaches
tension headaches migraines cluster headaches
32
anti-depressants
tricyclics & SNRI will reduce NE uptake & help reduce neurotransmitters in nociception (amitriptyline & venlafaxine)
33
chronic pain
LONG-LIVED acute pain where patients can accommodate to the physiological response - CAN OFTEN LEAD TO DEPRESSION AND ANXIETY
34
what causes migraine headaches?
- can be genetic somewhat, often associated w/ LOW estrogen levels - thought to be vascular (too much vasodilation in cranial vessels) but NOW, believed to be more neurogenic, involving neurons from the trigeminal nerve leading to vasodilation of meningeal blood vessels, release of inflammatory agents, more dilation, then headache
35
what causes tension headaches?
- thought to be due to muscle tone in pericardial region - often associated with sleep deprivation, smoking, cessation - if treated too often, can lead to MOH (medication Overuse Headache)
36
types of pain
nociceptive neuropathic acute chronic
37
Q: quality
what does it feel like?
38
T: temporal patterns
is it constant? intermittent?
39
Prophylaxis of migraines
- 1st line: Beta blockers (propanolol, metoprolol, atenolol, etc) or tricyclic antidepressants (imipramine, nortriptyline, amitriptyline) anticonvulsants (valproic acid, topiramate) Calcium Channel Blockers
40
neuropathic pain
from CNS processing following insult from disease or trauma such as: tingling, burning, shooting, etc.,
41
Muscle relaxants
likely only used when pain is related to muscle spasm
42
Rescue agent?
opioids such as: butorphanol or codeine can be used
43
U: you
how does it affect you?
44
nociceptive pain
from stimulation of neurons following injury, disease of inflammation of tissue - can be somatic (muscle, skin, or bone associated) - can be visceral (organ associated)